We will beat Alzheimer's on two fronts, and soon

Understanding dementia is hard; curing it is harder. But, fingers crossed, we
are just years away

Elderly patientPhoto: Alamy

By John Hardy, Chair of Molecular Biology of Neurological Disease at UCL

7:00AM GMT 21 Jan 2016

Alzheimer’s is one of the great challenges of our age. Reports this week have served to remind us that as our society ages, and more and more people develop the disease, immense strains will be placed on our health system and, of course, families who see loved ones drift away from them.

The trial may have worked slightly, though not well enough for us to be certain. It is now being retested

Alzheimer’s is also one of the great scientific challenges for medical researchers like me. I have worked on finding a cure for decades, currently at University College London. Last November I was honoured to become one of six scientists to receive a £2 million “Breakthrough Prize”. They are referred to as the “oscars” of the science world, but I didn’t even own a tuxedo before the black-tie ceremony. I am more a jeans and T-shirt type.

The prize was for the work I have been doing with my team on genetic mutations that give rise to early-onset Alzheimer’s.

It is the latest development in my understanding of a condition on which I first made a breakthrough back in 1990, at Imperial College London, when my team discovered how a protein called amyloid forms into sticky clumps, or plaques, around nerve endings. Genetic work from our group showed that in a few families this amyloid is where the disease started, and since we made that finding most drug company trials have aimed at this amyloid build up.

So far there have been six shots on this goal: four have been off target, that is they did not strike the amyloid. Two were on target, but one did not work. The other, however, may have worked slightly, though not well enough for us to be certain. It is now being retested. Clearly, we need more shots at the amyloid, and other drug trials are planned.

Recently, however, my team and another in Cardiff have come to realise that it is not just the amyloid build-up that matters, but how the brain reacts to it. So now we also have a second medical goal – helping the brain cope with the amyloid build-up better. Again, drug companies and academics, in Britain supported by Alzheimer Research UK and the Alzheimer Society, are trying to start drug trials aimed at this new target. These are not undertaken lightly. Each costs many millions.

The good news, and something Britain can be proud of, is that this country leads the world in many crucial areas of dementia research – notably genetics, epidemiology and pathology. Last November the Government also committed £150 million to fund a national dementia research institute. Yet we lag behind in other research areas such as cell biology, or animal modelling, partly because of anti-vivisection legislation.

How far are we from a cure? I’m afraid to say that it is still a lot easier to understand what’s going wrong in a brain affected by Alzheimer’s disease – difficult as this is – than it is to fix it. We are making steady progress in our understanding of the condition. That is encouraging. The problem is turning that understanding into treatment.

What is clear is that in most complicated diseases, such as diabetes, we take multiple drugs to combat different facets of that disease’s assault on our bodies. This is where we are heading in Alzheimer’s disease too; patients will end up taking both anti-amyloid drugs and drugs which help the brain protect itself. I am hopeful we will start on this road in the next five years.